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Article: α-Synuclein knockdown attenuates MPP+ induced mitochondrial dysfunction of SH-SY5Y cells

Titleα-Synuclein knockdown attenuates MPP<sup>+</sup> induced mitochondrial dysfunction of SH-SY5Y cells
Authors
Keywordsα-Synuclein
Mitochondrial dysfunction
Parkinson's disease
Short hairpin RNA
Issue Date2009
Citation
Brain Research, 2009, v. 1292, p. 173-179 How to Cite?
Abstractα-Synuclein is one of the main constituents of Lewy bodies and plays an important role in the pathology of Parkinson's disease. Mutation or overexpression of α-synuclein causes Parkinson's disease, and downregulation of α-synuclein resists MPP+-induced cell death, but the mechanism remains elusive. In this study, we attempted to explore the effect of α-synuclein knockdown on mitochondrial function in MPP+-treated SH-SY5Y cells. We reconstructed the short hairpin RNA expression vector, pGenesil-2, specially targeting α-synuclein mRNA, and it was stably transfected into SH-SY5Y cells. Cell viability, nuclear morphology, and mitochondrial membrane potential were then detected, and the expression of α-synuclein, cytochrome c, Bcl-2 and Bax were analyzed by Western blotting. The results showed that after exposure to 500 μM MPP+ for 24 h, about 41.0 ± 1.5% control cells showed low mitochondrial membrane potential. However, the percentage was 13.6 ± 1.2% in MPP+ treated α-synuclein knockdown cells. MPP+ induced cytochrome c release significantly, which was about 3.1-fold compared with that of control. However, in α-synuclein knockdown cells, the release of cytochrome c was blocked, which was about 1.4-fold compared with that of control. The Bcl-2/Bax ratio of SH-SY5Y cells reduced to 35.5 ± 3.8% after MPP+ treatment, and this ratio was 85.2 ± 3.0% in MPP+ treated α-synuclein knockdown cells. These data suggest that knockdown of α- synuclein might be an effective means in rescuing MPP+-induced mitochondrial dysfunction of SH-SY5Y cells. © 2009 Elsevier B.V. All rights reserved.
Persistent Identifierhttp://hdl.handle.net/10722/324938
ISSN
2021 Impact Factor: 3.610
2020 SCImago Journal Rankings: 1.037
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorWu, Fengxia-
dc.contributor.authorPoon, Wai Sang-
dc.contributor.authorLu, Gang-
dc.contributor.authorWang, Ancong-
dc.contributor.authorMeng, Haiwei-
dc.contributor.authorFeng, Lei-
dc.contributor.authorLi, Zhenping-
dc.contributor.authorLiu, Shuwei-
dc.date.accessioned2023-02-27T07:28:24Z-
dc.date.available2023-02-27T07:28:24Z-
dc.date.issued2009-
dc.identifier.citationBrain Research, 2009, v. 1292, p. 173-179-
dc.identifier.issn0006-8993-
dc.identifier.urihttp://hdl.handle.net/10722/324938-
dc.description.abstractα-Synuclein is one of the main constituents of Lewy bodies and plays an important role in the pathology of Parkinson's disease. Mutation or overexpression of α-synuclein causes Parkinson's disease, and downregulation of α-synuclein resists MPP+-induced cell death, but the mechanism remains elusive. In this study, we attempted to explore the effect of α-synuclein knockdown on mitochondrial function in MPP+-treated SH-SY5Y cells. We reconstructed the short hairpin RNA expression vector, pGenesil-2, specially targeting α-synuclein mRNA, and it was stably transfected into SH-SY5Y cells. Cell viability, nuclear morphology, and mitochondrial membrane potential were then detected, and the expression of α-synuclein, cytochrome c, Bcl-2 and Bax were analyzed by Western blotting. The results showed that after exposure to 500 μM MPP+ for 24 h, about 41.0 ± 1.5% control cells showed low mitochondrial membrane potential. However, the percentage was 13.6 ± 1.2% in MPP+ treated α-synuclein knockdown cells. MPP+ induced cytochrome c release significantly, which was about 3.1-fold compared with that of control. However, in α-synuclein knockdown cells, the release of cytochrome c was blocked, which was about 1.4-fold compared with that of control. The Bcl-2/Bax ratio of SH-SY5Y cells reduced to 35.5 ± 3.8% after MPP+ treatment, and this ratio was 85.2 ± 3.0% in MPP+ treated α-synuclein knockdown cells. These data suggest that knockdown of α- synuclein might be an effective means in rescuing MPP+-induced mitochondrial dysfunction of SH-SY5Y cells. © 2009 Elsevier B.V. All rights reserved.-
dc.languageeng-
dc.relation.ispartofBrain Research-
dc.subjectα-Synuclein-
dc.subjectMitochondrial dysfunction-
dc.subjectParkinson's disease-
dc.subjectShort hairpin RNA-
dc.titleα-Synuclein knockdown attenuates MPP<sup>+</sup> induced mitochondrial dysfunction of SH-SY5Y cells-
dc.typeArticle-
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.doi10.1016/j.brainres.2009.07.067-
dc.identifier.pmid19646423-
dc.identifier.scopuseid_2-s2.0-69449100026-
dc.identifier.volume1292-
dc.identifier.spage173-
dc.identifier.epage179-
dc.identifier.isiWOS:000270482900017-

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